Objective: To observe the expression of uncoupling protein (UCP2) and its effect on modulation of mitochondrial function and apoptosis of cardiomyocytes exposed to high-glucose.
Methods: AC16 cardiomyoctyes were randomly divided into normal-glucose group (NG), high-glucose group (HG), HG+ UCP2 siRNA group and HG+ negative control siRNA group.The expression of UCP2, succinodehydrogenase(SDH) activity, ATP content, reactive oxygen species (ROS) generation, cell apoptotic rate, caspase-3 activity and cell viability were detected.
Results: Compared with the cardiomyocytes in NG group, the ROS production, apoptotic rate and caspase-3 activity were significantly increased in HG group, accompanying with the decreases in SDH activity, ATP content and cell viability.The expression of UCP2 was increased in HG group. Furthermore, UCP2 siRNA inhibited the expression of UCP2 and aggravated high-glucose induced the ROS production (37.96±1.08 vs 27.68±0.60, P<0.05), cell apoptosis ((25.68±0.78)% vs (17.80±0.99)%, P<0.05), caspase-3 activity ((2.71±0.13)% vs (2.14±0.28)%, P<0.05) and cell inactivation (0.74±0.04 vs 0.62±0.03, P<0.05), but had no impact on SDH activity and ATP content in cardiomyocytes.
Conclusion: The up-regulation of UCP2 expression in cardiomyocytes, induced by high-glucose, maybe a protective mechanism for the mitochondrial damage, and UCP2 may inhibit high-glucose induced cardiomyocytes apoptosis.